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A Novel Triplet of Alisertib Plus Ibrutinib Plus Rituximab Is Active in Mantle Cell Lymphoma.
Cancers (Basel)
December 2024
Division of Hematology/Oncology, Department of Medicine, Mays Cancer Center, University of Texas Health San Antonio, San Antonio, TX 78229, USA.
: Aurora (AK) A/B are oncogenic mitotic kinases that when over-expressed are poor prognostic markers in mantle cell lymphoma (MCL). : Alisertib, an AK-A inhibitor, has anti-tumor activity in relapsed/refractory (r/r) MCL patients. We evaluated alisertib plus ibrutinib in MCL to abrogate ibrutinib resistance.
View Article and Find Full Text PDFInhibition of proteolytic and ATPase activities of the proteasome by the BTK inhibitor CGI-1746.
iScience
November 2024
Department of Drug Discovery and Development, Harrison College of Pharmacy, Auburn University, 720 S. Donahue Dr., Auburn, AL, USA.
Bruton's tyrosine kinase (BTK) inhibitor, ibrutinib, has been shown to synergize with proteasome inhibitors (PIs) in reducing the viability of cells derived from B cell malignancies, but the mechanism is not known. We report here that an off-target effect of ibrutinib causes synergy because not all BTK inhibitors exhibited the synergistic effect, and those that synergized did so even in cells that do not express BTK. The allosteric BTK inhibitor CGI-1746 showed the strongest synergy.
View Article and Find Full Text PDFPharmacological Management of IgG4-Related Disease: From Traditional to Mechanism-Based Targeted Therapies.
Drugs Aging
January 2025
Division of Rheumatology, Department of Internal Medicine, Keio University School of Medicine, 35 Shinanomachi, Shinjuku-ku, Tokyo, 160-8582, Japan.
IgG4-related disease (IgG4-RD) is an immune-mediated disorder characterized by organ enlargement and dysfunction. The formation of tertiary lymphoid tissues (TLTs) in affected organs is crucial for understanding IgG4-RD, as T follicular helper (Tfh) 2 cells within TLTs drive IgG4+B cell differentiation, contributing to mass formation. Key cytokines IL-4 and IL-10, produced by Tfh2 cells, are essential for this process.
View Article and Find Full Text PDFInhibition of Bruton's tyrosine kinase restricts neuroinflammation following intracerebral hemorrhage.
Theranostics
January 2025
Department of Neurology, Tianjin Neurological Institute, Tianjin Institute of Immunology, State Key Laboratory of Experimental Hematology, International Joint Laboratory of Ocular Diseases, Ministry of Education, Haihe Laboratory of Cell Ecosystem, Laboratory of Post-Neuroinjury Neurorepair and Regeneration in Central Nervous System Tianjin & Ministry of Education, Tianjin Medical University General Hospital, Tianjin 300052, China.
Intracerebral hemorrhage (ICH) is a devastating form of stroke with a lack of effective treatments. Following disease onset, ICH activates microglia and recruits peripheral leukocytes into the perihematomal region to amplify neural injury. Bruton's tyrosine kinase (BTK) controls the proliferation and survival of various myeloid cells and lymphocytes.
View Article and Find Full Text PDFFungal infection in patients treated with Bruton's Tyrosine Kinase inhibitor, from epidemiology to clinical outcome: A systematic review.
Clin Microbiol Infect
December 2024
Sorbonne Université, CIMI-Paris, AP-HP, Service de Parasitologie-Mycologie, Hopital de La Pitie-Salpetriere, F-75013 Paris, France. Electronic address:
Background: Bruton Tyrosine Kinase inhibitor (BTKi) emerged as key treatment for B-cell lymphomas. Despite its efficacy in the treatment of malignancies, numerous cases of invasive fungal infections (IFI) have been reported in patients receiving ibrutinib, a first generation BTKi. Cases of invasive aspergillosis have also been reported with acalabrutinib and zanubrutinib.
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